In terminal SIV infection in macaques, lentivirus-infected leukocytes are numerous in SIV-specific infiltrates yet are rarely detected at inflammatory sites associated with opportunistic infections. This refutes the theory that opportunistic infections during HIV/SIV infection serve as a stimulus for the recruitment of lentivirus-infected cells. However, during acute SIV-infection we have observed occasional animals with SIV-positive leukocytes associated with Pneumonyssus-induced granulomas. Our hypothesis is that SIV-infected leukocytes are able to traffic to inflammatory sites early in infection, but lose this ability late in disease. We induced granulomas in three uninfected and three late-stage SIV-infected macaques by subcutaneous injection of complete Freunds adjuvant. Seven days post-CFA injection (pCFA), uninfected animals were infected IV with SIV. At days 13 and 25 pCFA, granulomas from all acutely infected animals had numerous SIV+ (SIV antigen and nucleic acid) leukocytes, while only one of three late-stage infected animals had any detectable virus. This animal was in the terminal stage of disease and despite high plasma antigenemia, had only rare SIV+ cells in the granuloma. Axillary lymph node biopsies at day 25 pCFA revealed comparable numbers of SIV+ cells between this animal and acutely infected animals. By day 35 pCFA, fewer SIV+ cells were in the granulomas in the acute group and only rare SIV+ positive cells were found in one terminally ill animal from the late-stage group. These results demonstrate defective trafficking of lentivirus-infected leukocytes